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Tags: Cardiac/drug effects/*enzymology

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Overexpressing superoxide dismutase 2 induces a supernormal cardiac function by enhancing redox-dependent mitochondrial function and metabolic dilation.

During heightened cardiac work, O2 consumption by the heart benefits energy production via mitochondria. However, some electrons leak from the respiratory chain and yield superoxide, which is rapidly metabolized into H2O2 by SOD2. To understand the…

Tags: 2015, Adenosine Triphosphate/biosynthesis, Animals, Arterial Pressure/drug effects, Bioenergetics, Blood Flow Velocity/drug effects, Cardiac function, Cardiac/drug effects/*enzymology, Catalase/pharmacology, Chen Chwen-Lih, Chen Yeong-Renn, Chilian William M, Department of Integrative Medical Sciences, Echocardiography, Female, Gene Expression, Heart/drug effects/*enzymology, Hydrogen Peroxide/*metabolism/pharmacology, Injections, Intravenous, Journal of molecular and cellular cardiology, Kang Patrick T, Luther Daniel J, Male, Meszaros J Gary, Metabolic dilation, Mice, Mitochondria, Myocardium/*enzymology, Myocytes, NEOMED College of Medicine, NG-Nitroarginine Methyl Ester/pharmacology, Ohanyan Vahagn, Oxidation-Reduction, Oxygen Consumption/drug effects, Redox regulation, Signal Transduction, Stroke Volume/drug effects, Superoxide dismutase 2 (SOD2), Superoxide Dismutase/*genetics/metabolism, Transgenic, Transgenic mice, Vasodilation/*drug effects

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